Leira R, Rodríguez-Yáñez M, Castellanos M, Blanco M, Nombela F, Sobrino T, Lizasoain I, Dávalos A, Castillo J
Department of Neurology, Stroke Unit and Neurovascular Research Laboratory, Hospital Clínico Universitario, Santiago de Compostela, Spain.
J Intern Med. 2006 Oct;260(4):343-9. doi: 10.1111/j.1365-2796.2006.01694.x.
The influence of temperature on the outcome observed in experimental models of ischaemic stroke has not been definitively proved in patients with stroke. Interleukin-6 (IL-6) acts as important endogenous pyrogen, and it is an important regulator of spontaneous body temperature during cerebral ischaemia. The objective of this study was to determine, during the acute phase of cerebral ischaemia, the potential relationship between proinflammatory cytokines and hyperthermia as a cause of larger cerebral infarcts.
We studied 229 patients with a first-ever acute hemispheric infarction admitted within the first 24 h from onset of symptoms. On admission, axillary temperature was recorded and blood chemistry studies and cranial computed tomography were performed. We classified body temperature into two groups: hyperthermia (>or=37.5 degrees C) and normothermia (<37.5 degrees C). We determined proinflammatory markers [IL-6, tumour necrosis factor-alpha (TNF-alpha), intercellular adhesion molecule (ICAM-1) and vascular cellular adhesion molecule] on admission. Two outcome variables were evaluated: (i) infarct volume; (ii) Canadian Stroke Scale (CSS) at 3 months (CSS <or= 7 was considered poor outcome and CSS > 7 good outcome).
Patients with hyperthermia had higher infarct volume [46.5 (9.8-78.5) cm(3) vs. 19.1 (5.0-23.5) cm(3); P < 0.0001], as well as poor outcome at 3 months. Plasma levels of IL-6, TNF-alpha and ICAM-1 were significantly higher in the group of patients with hyperthermia than in the normothermic group. There was a significant correlation between body temperature on admission and infarct volume (r = 0.302; P < 0.0001), and between proinflammatory markers (IL-6 and TNF-alpha) and infarct volume. A significant association was also found between proinflammatory markers (IL-6, TNF-alpha, and ICAM-1) and poor outcome. However, after adjustment for potential confounders, hyperthermia was not independently associated with either larger infarct volume or with poor outcome at 3 months.
Inflammatory mediators play a role in acute ischaemic brain damage independently of hyperthermia.
温度对缺血性中风实验模型中观察到的结果的影响在中风患者中尚未得到明确证实。白细胞介素-6（IL-6）作为重要的内源性致热原，是脑缺血期间体温自发调节的重要调节因子。本研究的目的是确定在脑缺血急性期，促炎细胞因子与体温过高作为更大脑梗死原因之间的潜在关系。
我们研究了229例首次急性半球梗死患者，这些患者在症状发作后的24小时内入院。入院时，记录腋温并进行血液化学研究和头颅计算机断层扫描。我们将体温分为两组：体温过高（≥37.5℃）和体温正常（<37.5℃）。我们在入院时测定促炎标志物[IL-6、肿瘤坏死因子-α（TNF-α）、细胞间黏附分子（ICAM-1）和血管细胞黏附分子]。评估两个结果变量：（i）梗死体积；（ii）3个月时的加拿大卒中量表（CSS）（CSS≤7被认为是预后不良，CSS>7是预后良好）。
体温过高的患者梗死体积更大[46.5（9.8 - 78.5）cm³对19.1（5.0 - 23.5）cm³；P < 0.0001]，并且3个月时预后不良。体温过高组患者的血浆IL-6、TNF-α和ICAM-1水平显著高于体温正常组。入院时体温与梗死体积之间存在显著相关性（r = 0.302；P < 0.0001），促炎标志物（IL-6和TNF-α）与梗死体积之间也存在显著相关性。促炎标志物（IL-6、TNF-α和ICAM-1）与预后不良之间也存在显著关联。然而，在对潜在混杂因素进行调整后，体温过高与3个月时更大的梗死体积或预后不良均无独立相关性。
炎症介质在急性缺血性脑损伤中发挥作用，与体温过高无关。
